ATM-NF-κB Connection as a Target for Tumor Radiosensitization

摘要: Ionizing radiation (IR) plays a key role in both areas of carcinogenesis and anticancer radiotherapy. The ATM (ataxia-telangiectasia mutated) protein, sensor to IR other DNA-damaging agents, activates wide variety effectors involved multiple signaling pathways, cell cycle checkpoints, DNA repair apoptosis. Accumulated evidence also indicates that the transcription factor NF-kappaB (nuclear factor-kappaB) critical cellular protection against genotoxic agents including IR, inhibition leads radiosensitization radioresistant cancer cells. was found be defective cells from patients with A-T (ataxia-telangiectasia) who are highly sensitive damage induced by UV lights. Cells derived individuals hypersensitive killing IR. Both deficiencies result increased sensitivity double strand breaks. Therefore, identification molecular linkage between kinase tumor response therapeutic will lead better understanding promise novel targets for therapy-associated resistance. This review article focuses on recent findings related relationship Also, association subunit p65 adaptive response, recently observed our lab, is discussed.